PDF(Pubmed)
Abstract：
Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease characterized by progressive loss of motor neurons. Emerging evidence suggests a potential link between metabolic dysregulation and ALS pathogenesis. This study aimed to investigate the relationship between metabolic hormones and disease progression in ALS patients. A cross-sectional study was conducted involving 44 ALS patients recruited from a tertiary care center. Serum levels of insulin, total amylin, C-peptide, active ghrelin, GIP (gastric inhibitory peptide), GLP-1 active (glucagon-like peptide-1), glucagon, PYY (peptide YY), PP (pancreatic polypeptide), leptin, interleukin-6, MCP-1 (monocyte chemoattractant protein-1), and TNFα (tumor necrosis factor alpha) were measured, and correlations with ALSFRS-R, evolution scores, and biomarkers were analyzed using Spearman correlation coefficients. Subgroup analyses based on ALS subtypes, progression pattern of disease, and disease progression rate patterns were performed. Significant correlations were observed between metabolic hormones and ALS evolution scores. Insulin and amylin exhibited strong correlations with disease progression and clinical functional outcomes, with insulin showing particularly robust associations. Other hormones such as C-peptide, leptin, and GLP-1 also showed correlations with ALS progression and functional status. Subgroup analyses revealed differences in hormone levels based on sex and disease evolution patterns, with male patients showing higher amylin and glucagon levels. ALS patients with slower disease progression exhibited elevated levels of amylin and insulin. Our findings suggest a potential role for metabolic hormones in modulating ALS progression and functional outcomes. Further research is needed to elucidate the underlying mechanisms and explore the therapeutic implications of targeting metabolic pathways in ALS management.
摘要：
肌萎缩侧索硬化(ALS)是一种以运动神经元进行性丧失为特征的破坏性神经退行性疾病。新出现的证据表明代谢失调和ALS发病机制之间存在潜在的联系。本研究旨在探讨ALS患者代谢激素与疾病进展的关系。进行了一项横断面研究，涉及从三级护理中心招募的44名ALS患者。血清胰岛素水平，总胰淀素,C-肽，活性生长素释放肽,GIP（抑胃肽），GLP-1活性（胰高血糖素样肽-1），胰高血糖素,PYY（肽YY），PP（胰腺多肽），瘦素,白细胞介素-6，MCP-1（单核细胞趋化蛋白-1），和TNFα（肿瘤坏死因子α）进行测量，以及与ALSFRS-R的相关性，进化分数，使用Spearman相关系数分析生物标志物。基于ALS亚型的亚组分析，疾病的进展模式，并进行了疾病进展率模式。在代谢激素和ALS进化评分之间观察到显着的相关性。胰岛素和胰淀素与疾病进展和临床功能结果具有很强的相关性，与胰岛素表现出特别强烈的关联。其他激素，如C肽，瘦素,和GLP-1也显示与ALS进展和功能状态相关。亚组分析显示基于性别和疾病演变模式的激素水平差异，男性患者胰淀素和胰高血糖素水平较高。疾病进展较慢的ALS患者表现出胰淀素和胰岛素水平升高。我们的研究结果表明，代谢激素在调节ALS进展和功能结局方面具有潜在作用。需要进一步的研究来阐明潜在的机制，并探索ALS管理中靶向代谢途径的治疗意义。
